Reduced ventricular flow propagation velocity in elite athletes is augmented with the resumption of exercise training
1 School of Human Movement and Exercise Science
2 School of Medicine and Pharmacology, University of Western Australia, Perth, Australia
3 Cardiac Transplant Unit, Royal Perth Hospital, Perth, Australia
4 Western Australian Institute of Sport, The Western Australian Institute for Medical Research, Perth, Australia
Abstract
Chronic exercise induces physiological enlargement of the left ventricle (‘athlete's heart’), but the effects of current and long-term exercise training on diastolic function have not been investigated. Echocardiography and Doppler imaging were used to assess left ventricular (LV) dimensions and indices of diastolic filling in 22 elite athletes at the end of their ‘off-season’ (baseline) and, subsequently, following 3 and 6 months of training. Twelve matched controls were also studied at baseline, 3 and 6 months. Compared to controls at baseline, athletes exhibited significantly higher LV mass (235.7 ± 7.1 g versus 178.1 ± 14.5 g, P < 0.01) and reduced flow propagation velocity (VP: 50.21 ± 1.7 versus 72.2 ± 3.6 cm s–1, P < 0.01), a measure of diastolic function. Three months of training further increased LV mass in athletes (253.2 ± 7.1 g; P < 0.01 versus baseline), and significantly increased their VP (66.7 ± 2.5 cm s–1; P < 0.05 versus baseline). These trends for increased mass and diastolic filling persisted following 6 months of training (LV mass 249.0 ± 8.7 g P < 0.05 versus baseline; VP 75.7 ± 3.0 cm s–1; P < 0.01 versus baseline, and P = 0.01 versus 3 months). This study suggests that following a period of relative inactivity the rate of ventricular relaxation during early diastole may be slowed in athletes who exhibit ventricular hypertrophy, whilst resumption of training increases the speed of ventricular relaxation in the presence of further hypertrophy of the left ventricle.
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Introduction
Vigorous exercise training induces hypertrophy of the left ventricle, an adaptation commonly referred to as ‘athlete's heart’ (Maron, 1986). In patients with cardiovascular disease, left ventricular (LV) hypertrophy is associated with diastolic dysfunction, characterized by impaired ventricular relaxation and filling which manifest on echocardiographic assessment as Doppler velocity abnormalities (Ommen & Nishimura, 2003). However, exercise training is cardioprotective, being associated with decreased cardiovascular mortality and morbidity in both primary (Paffenbarger et al. 1993; Blair et al. 1995) and secondary prevention settings (Joliffe et al. 2003) and, in contrast with the situation in patients with cardiovascular disease, LV hypertrophy associated with athletic training is likely to be a benign or beneficial adaptation which does not impact on ventricular relaxation in the same manner as ‘pathological’ hypertrophy. Previous studies indicate that, despite significant ventricular hypertrophy, athletes possess normal (MacFarlane et al. 1991; Yeater et al. 1996) or enhanced diastolic function (Douglas et al. 1986; George et al. 1999; Caso et al. 2000), compared to matched controls. However, these studies relied exclusively upon cross-sectional comparisons and, to our knowledge, no studies have investigated changes in LV diastolic function in athletes studied longitudinally in response to exercise training. The purpose of the current study was therefore to assess cardiac structural and functional adaptations to exercise training in elite level athletes across a typical training cycle, which is at the end of the ‘off-season’ and following 3 and 6 months of intensive training.
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Methods
Subject characteristics
Twenty-two elite rowers (17 male, 5 female) from the West Australian Institute of Sport were recruited into the ‘athlete’ group. The characteristics of these subjects were as follows (mean ± S.E.M.): age 20.4 ± 0.7 years, height 186.2 ± 1.0 cm, weight 81.5 ± 1.8 kg, body surface area (BSA) 2.06 ± 0.03 m2, mean resting heart rate (HR) 56 ± 2 b.p.m., resting systolic (SBP) 122 ± 2 mmHg, and resting diastolic blood pressure (DBP) 78 ± 2 mmHg.
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Twelve healthy controls matched for sex (8 male, 4 female), age 21.8 ± 1.1 years, height 183.9 ± 1.9 cm, weight 76.2 ± 3.1 kg, BSA 1.97 ± 0.04, resting HR 59 ± 2 b.p.m., SBP 123 ± 2 mmHg, and DBP 74 ± 3 mmHg, were recruited from the University of Western Australia for comparison.
Inclusion criteria for the athlete group were previous competition at national or international level, and inclusion in the Western Australian Institute of Sport elite rowing squad. Healthy controls were defined as individuals undertaking less than 3 h of regular exercise per week. All participants were screened for cardiac abnormalities and cardiovascular disease prior to entering the study. Subjects who smoked, were hypertensive, had a family history of hypertrophic occlusive cardiomyopathy or were on medications of any type were excluded, as were athletes on performance enhancing drugs.
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The study procedures were approved by the Ethics Committee of Royal Perth Hospital and all subjects gave written consent. The study conformed to the Declaration of Helsinki.
Experimental design
Athletes entered the study (baseline measures) at the beginning of their training cycle, that is, following the end of a 6 week ‘off season’ during which all formal training was suspended. Interviews were conducted to confirm that the athletes had not been training or exercising regularly during this ‘off-season’ phase; none of the subjects continued on-water training, 13 reported undertaking no exercise whatsoever, whilst the remaining nine performed relatively low intensity activity, none for more than 4 h per week; four reported undertaking intermittent jogging and five undertook school-based sport. To assess the effect of resumption of training, all measures were repeated following 3 and 6 months of training. Training in the athletes consisted of two sessions of exercise per day, 6–7 days per week. Morning sessions were ‘on water’ and consisted of 2.5 h training at, or near, competition pace, i.e. approx. 80–90% maximum heart rate (HRmax). Afternoon sessions were 2 h in duration and consisted of general aerobic conditioning (e.g. 12 km timed runs) or resistance training (80–90% 1RM (repetition maximum), 6–8 repetitions).
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The controls were recreationally active and healthy but did not undertake formal training for any sport, and their activity levels remained constant throughout the duration of the study. Data for the control group were collected at baseline, 3 months and 6 months to coincide with data collection in the athlete group.
Experimental measures
Two-dimensional ultrasound imaging, M-mode imaging and pulsed wave Doppler and flow propagation velocity (VP) measurements were used to assess resting cardiac structure and function in each subject. All measurements were performed following a 4-h fast, abstinence from caffeine and/or alcohol for 12 h and at least 18 h after physical activity. Echocardiographic assessments were collected and analysed by a trained sonographer (L.H.N.), who was not blinded. To check for systematic bias, a random sample of 30 of these scans were also assessed by a specialist echocardiologist (J.A.D.) who was uninformed as to subject group and session and had no direct contact with the subjects.
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Measures of cardiac structure. Left ventricular dimensions were measured using two-dimensional guided M-mode measurements on an ultrasound machine (Aspen, Acuson, Mountain View, CA, USA) equipped with a 2.5 MHz multiarray transducer. The mean value of at least five measurements of each dimension of the left ventricle was determined: interventricular septal thickness (IVS), left ventricular diastolic dimension (LVIDd), posterior wall thickness (PWT) and left ventricular systolic dimension (LVIDs). Left ventricular mass was calculated according to the recommendations of the American Society of Echocardiography (ASE):
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LV mass was indexed to BSA to calculate LV mass index (LVMi). Relative wall thickness (RWT), an indicator of LV geometry, often used to discriminate between different forms of LV hypertrophy (Roman et al. 1992), was calculated as 2 x (PWT/LVIDd).
Measures of cardiac systolic function. Stroke volume (SV), ejection fraction (EF) and fractional shortening (FS) were calculated using M-mode imaging to assess global function of the LV. Fractional shortening was estimated as the difference between systolic and diastolic ventricular dimensions (normalized to diastolic LVIDd). Stroke volume and EF were calculated from estimated LV volumes, with:
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Measures of cardiac diastolic function. The primary measure for diastolic function was colour M-mode Doppler flow propagation velocity (VP). VP measurements were obtained from apical four-chamber views, with the M-mode cursor as parallel as possible to flow obtained by colour Doppler, and the Doppler colour scale adjusted for aliasing. VP was recorded at a sweep speed of 100 mm s–1 and measured as the slope of first aliasing velocity in centimetres per second, with normal VP ranging between 68 and 105 cm s–1 (Anderson, 2000).
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Transmitral flow measurements were also made according to the ASE guidelines (Quinones et al. 2002; Gottdiener et al. 2004) and used as a secondary measure of diastolic function. Transmitral peak early filling velocity (Peak E), the deceleration time of early flow (DT) and peak velocity of atrial filling (Peak A) were measured, and the E/A ratio calculated.
Peak systolic (Peak S) and diastolic (Peak D), and atrial reversal (AR) velocities were also measured and the S/D ratio calculated from pulsed Doppler measures in the right upper pulmonary vein.
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Statistical analysis
Student's unpaired t test was used to assess significance between the controls and rowers at baseline. Two-way ANOVA was used to assess significance of difference (P < 0.05) between the athletes and controls across the three time points. One-way ANOVA was used within groups to determine whether variables changed with training, or across the non-training period in the case of controls. Where ANOVA revealed significant differences, post hoc t tests were used to compare individual time points. All data are reported as means ± S.E.M. and statistical significance was assumed at P < 0.05. All statistical analysis was performed using SPSS, version 11.0 (SPSS Inc., Chicago, IL, USA). Sub-group analysis on the male athletes revealed similar data to the group as a whole, so all data were pooled.
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The coefficient of variation (CV) for our primary outcome variable, VP, was 9.9%. This was calculated via assessment of the standard deviation of the differences between paired measurements at baseline and 3 months in the control subjects, division of this value by the square root of 2, and expression as a percentage of the mean value.
Results
Baseline cardiac structure
Compared to controls, athletes possessed structural adaptations consistent with ‘athlete's heart’; that is, increased LV mass (P < 0.01; Table 1, Fig. 1), with underlying increases in cavity dimension (LVIDd P < 0.01) and wall thicknesses (IVS and PWT, P < 0.01), but no significant differences in RWT between the groups (Table 1).
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Values are means ± S.E.M. The athletes possessed significantly increased LV mass (all P < 0.001) compared to the controls at all three time points. Compared to baseline measures, LV mass increased following 3 and 6 months training in the athlete group (P < 0.01, P < 0.05, respectively), but no changes occurred in LV mass in controls with time. *P < 0.001; P < 0.01; P < 0.05.
Baseline cardiac function
Stroke volume (SV) was the only measure of cardiac systolic function which significantly differed between athletes and controls at baseline (95.05 ± 2.78 ml versus 81.88 ± 2.53 ml; P < 0.05). Other indices of global LV systolic function were within normal ranges for both groups, with EF of 70 ± 1% and 72 ± 2% (athletes versus controls, not significant (NS)) and FS 39 ± 1% versus 42 ± 1% (NS).
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In terms of diastolic function, our primary measure (colour M-mode flow propagation velocity, VP) showed the largest differences between the groups at baseline (P < 0.001, Table 2), suggesting reduced diastolic filling parameters in the athletes. This was supported by increased deceleration times (DT; P < 0.01) with 10 athletes having DT measures greater than that defined as ‘normal’ (258 ms) (Munagala et al. 2003), whereas this was the case in only one control subject. The atrial reversal (AR) measured at the pulmonary veins also supported reduced diastolic parameters (P < 0.01). However, the E/A ratio, a preload dependent index (Ommen & Nishimura, 2003), which we measured purely to provide comparisons with previously published data, did not show any differences between groups (Table 2). Furthermore, the E/A ratio has been shown only to be accurate in predicting LV diastolic function in patients with systolic dysfunction, is non-specific and is influenced by many other factors, particularly in patients with preserved systolic function (such as this group of athletes) (Nishimura et al. 1996; Yamamoto et al. 1997).
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Effects of exercise training on cardiac structure
The athletes were highly motivated and compliance to the training program was excellent (98% across the period of the study, with no individual missing more than 20 out of 288 sessions). increased from 5.51 ± 0.20 at baseline to 5.64 ± 0.22 at 3 months and 5.68 ± 0.20 l min–1 at 6 months (both 3 and 6 months versus baseline P < 0.01).
Two-way ANOVA between athletes and controls at baseline and 3 months revealed significant differences in all indices of cardiac ‘structure’ (Table 1). This was indicated by increased measures in the athletes of LV mass, LVMi, IVS, PWT, and LVIDs following 3 months of training (Table 1). These findings were also evident following 6 months; LV mass, IVS, LVIDs and RWT remained significantly elevated relative to baseline measures (all P < 0.05). There were no significant differences in any measures of cardiac structure between the three time points in the control subjects.
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Effects of exercise training on cardiac function
Systolic function was not significantly altered by training in the athletes or across time in the control subjects (SV, SV index, EF and FS, all NS). However, indices of diastolic function were significantly augmented with the resumption of training, at 3 months VP, the S/D ratio and AR all differed compared to baseline measures (P < 0.05; Table 2, Fig. 2). Similar findings were evident for VP and AR following 6 months (P < 0.01; Table 2).
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Values are means ± S.E.M. The athletes possessed impaired VP compared to the controls at baseline (P < 0.001). VP improved with 3 months of training (P < 0.05 compared to controls), and normalized (NS, compared to controls) following 6 months of training. There were significant improvements in VP in the athlete group from baseline to 3 months (P < 0.001) and 6 months (P < 0.001), and from 3 to 6 months (P < 0.001). *P < 0.001; P < 0.01; P < 0.05.
At 3 months the athletes had significantly different VP, DT and S/D ratio measurements compared to the controls (all P < 0.05; Table 2). Following 6 months of training, there were no differences in any measures of diastolic function between the athletes and controls. There were no significant changes in any of the measures of diastolic function in controls between baseline, 3 or 6 months.
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Two-way ANOVA performed across the three study time-points between athletes and controls revealed a significant interaction term for VP (P < 0.001) and significant time (P < 0.05) and group (P < 0.0001) differences for LV mass.
Discussion
Our results indicate that athletes who are not currently active possess evidence of delayed early diastolic ventricular relaxation in concert with increased cardiac dimensions compared to matched controls. Following resumption of training for 3 months, we observed further increase in cardiac structure in the athletes, associated with augmented indices of diastolic relaxation. These changes persisted following 6 months of training, with measures of early diastolic filling reaching levels no longer statistically different from controls.
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Several previous studies have reporting increased cardiac dimensions (MacFarlane et al. 1991; Spirito et al. 1994; George et al. 1999; Pelliccia et al. 1999) in athletes. However, these studies used cross-sectional comparisons and the effects of training on cardiac structure and diastolic function in individual athletes remain unknown. We observed significantly increased LV dimensions and mass in athletes, which was further augmented following resumption of training. Our results also indicate increased SV in the presence of normal EF, reflecting the enlarged LV dimensions in athletes. These wall thickening and cavity enlargement results in rowers concur with previous cross-sectional comparisons in the literature (Finkelhor et al. 1986; Urhausen et al. 1996; Pelliccia & Maron, 1997; Pelliccia et al. 1999; Pelliccia et al. 2002), including a study which suggested that LV hypertrophy persists after long-term detraining in elite athletes (Pelliccia et al. 2002). It is interesting to note in the present study that, despite marked physiological hypertrophy relative to matched controls at the end of the ‘off-season’ in athletes, resumption of training induced further, significant increases in LV mass. This finding is consistent with a recent study which assessed serial left ventricular structural adaptations in cyclists (Abergel et al. 2004), indicating that individuals with existing evidence of ‘athlete's heart’ can undergo further cardiac enlargement as a result of the further exercise training.
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We describe, for the first time, reduced flow propagation velocity in athletes following their ‘off-season’. Although all measures of diastolic function are preload dependent, VP is relatively insensitive to changes in preload (Brun et al. 1992; Garcia et al. 1999) compared to the E/A ratio (Gottdiener et al. 2004) and tissue Doppler echocardiographic (TDI) indices (Firstenberg et al. 2001) and correlates closely with (Garcia et al. 2000), the time constant for isovolumetric ventricular relaxation. This reduction in VP relative to controls, supported by transmitral DT and pulmonary venous AR measures, indicates that the enlarged LV dimensions evident in athletes are associated with delayed diastolic filling when athletes are not currently engaged in training. Furthermore, our findings indicate that resumption of physical activity results in improvement in diastolic filling in athletes, in the presence of further cardiac enlargement and wall thickening. Previous reports, which have predominantly undertaken cross-sectional comparisons between athletes and controls using the E/A ratio, have interpreted their data as indicating either normal or enhanced diastolic function in athletes (Douglas et al. 1986; MacFarlane et al. 1991; George et al. 1999). Our data are not entirely inconsistent with these studies, as exercise training significantly improved VP in the athletes and the athletes possessed similar diastolic function to controls when they were training. Nonetheless, our finding of delayed early diastolic filling in athletes at entry, when they were relatively inactive, differs from previous studies which have reported enhanced diastolic function. Several possible explanations exist for the disparity. Firstly, all previous studies have utilized cross-sectional designs and have not specifically reported at what stage of the training cycle athletes were studied. This is relevant given our VP data strongly indicate that early diastolic filling was initially reduced when the athletes were not active, whereas progressive normalization occurred with training. A second possible explanation may relate to the indices of diastolic function used. Previous studies have typically relied upon the E/A ratio, which has several important limitations including preload dependence (Ommen & Nishimura, 2003), which may be of particular relevance in athletes in whom plasma volume and preload may be enhanced by training.
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Whilst the Doppler measures we report in this paper are typically those assessed in the clinical setting (Gottdiener et al. 2004), we think it unlikely that the impaired VP, DT and AR data we observed in the inactive athletes are indicative of diastolic dysfunction in these subjects, who are young, healthy and capable of performing at extremely high levels. We do not have evidence that the heart fills inadequately, or at higher pressures than normal or that it cannot sustain higher levels of venous return during exercise and it would therefore be inappropriate to infer diastolic ‘dysfunction’ from the clinical setting. Furthermore, previous studies indicate that exercise training improves ventricular compliance (Levine et al. 1991) and, although chronic inactivity associated with bed rest and space flight are associated with impaired compliance (Perhonen et al. 2001a; Perhonen et al. 2001b), this degree of activity restriction is not relevant to our study. Ultimately though, our data do indicate that propagation velocity is slowed following a period of detraining and raise interesting questions regarding mechanisms. Propagation velocity is dependent upon atrioventricular pressure gradients, the relationship between end-systolic volume and equilibrium volume and the rate of relaxation in early diastole. It is possible that any or all of these determinants were altered in the present study; for example, decreased plasma volume as a consequence of detraining, in the presence of sustained ventricular enlargement, may have decreased equilibrium volume to the point where early diastolic suction and flow propagation were decreased. This explanation is speculative and others may exist; future studies incorporating new and evolving technologies, such as myocardial tissue Doppler imaging and cardiac MRI will provide further valuable information regarding the effects of exercise on LV structure and diastolic filling. Functional assessment of ventricular compliance and construction of Starling curves (Levine et al. 1991) during different phases of athletic training cycles would be particularly revealing, although ethical concerns in elite athletes may limit such invasive investigations.
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There are several limitations of the present study. It is well established that Doppler measures of diastolic function are HR dependent and training-induced changes or differences between controls and athletes may be partly dependent upon differences in HR. However, the athletes and controls were well matched for resting HR and no significant changes in HR were observed across the training programme in the athletes. Furthermore, the slight decrease in resting HR with training in the athletes would not be expected to increase VP, as observed at 3 and 6 months. A second possible limitation relates to the measures of diastolic function we reported. As mentioned above, we have attempted to present those measures which we believe are the most valid, given the limitations of Doppler approaches. VP is the Doppler approach recommended to assess diastolic function by the American Society of Echocardiography as it is less subject to ‘pseudonormalization’ and correlates better with than other measures (Garcia et al. 2000; Gottdiener et al. 2004). Furthermore, VP appears less preload dependent than tissue Doppler measures (Garcia et al. 2000; Firstenberg et al. 2001). Finally, several echocardiographic approaches exist to assess LV mass. We adopted the algorithm recommended for use in conjunction with linear measures of ventricular wall thickness and cavity dimensions (Gottdiener et al. 2004). Such measures are subject to limitations associated with oblique parasternal imaging, but in subjects with normal geometry the approach we adopted is preferred to the use of Simpson's rule due to difficulty identifying boundaries of the LV free wall from base to apex in apical windows (Gottdiener et al. 2004). Reproducibility of the approach we used is acceptable given careful attention to image quality and assessment of primary dimensions (Gottdiener et al. 2004) and we think it unlikely that the relatively small training-induced change in LV mass we observed in athletes is the result of a type 2 error as both the 3 and 6 month data increased consistently and no change was observed in the parallel control group over time. Furthermore, the magnitude of increase in LV mass we report is similar to, or greater than, that previously reported as significant as a result of other interventions (Poppas et al. 1997; Mesa et al. 1999; Modena et al. 1999; Mayet et al. 2000).
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In summary, data from the present study imply that following a period of relative inactivity, the rate of ventricular relaxation during early diastole may be slowed in athletes who exhibit ventricular hypertrophy, whilst resumption of training increases the speed of ventricular relaxation in the presence of further hypertrophy of the LV.
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2 School of Medicine and Pharmacology, University of Western Australia, Perth, Australia
3 Cardiac Transplant Unit, Royal Perth Hospital, Perth, Australia
4 Western Australian Institute of Sport, The Western Australian Institute for Medical Research, Perth, Australia
Abstract
Chronic exercise induces physiological enlargement of the left ventricle (‘athlete's heart’), but the effects of current and long-term exercise training on diastolic function have not been investigated. Echocardiography and Doppler imaging were used to assess left ventricular (LV) dimensions and indices of diastolic filling in 22 elite athletes at the end of their ‘off-season’ (baseline) and, subsequently, following 3 and 6 months of training. Twelve matched controls were also studied at baseline, 3 and 6 months. Compared to controls at baseline, athletes exhibited significantly higher LV mass (235.7 ± 7.1 g versus 178.1 ± 14.5 g, P < 0.01) and reduced flow propagation velocity (VP: 50.21 ± 1.7 versus 72.2 ± 3.6 cm s–1, P < 0.01), a measure of diastolic function. Three months of training further increased LV mass in athletes (253.2 ± 7.1 g; P < 0.01 versus baseline), and significantly increased their VP (66.7 ± 2.5 cm s–1; P < 0.05 versus baseline). These trends for increased mass and diastolic filling persisted following 6 months of training (LV mass 249.0 ± 8.7 g P < 0.05 versus baseline; VP 75.7 ± 3.0 cm s–1; P < 0.01 versus baseline, and P = 0.01 versus 3 months). This study suggests that following a period of relative inactivity the rate of ventricular relaxation during early diastole may be slowed in athletes who exhibit ventricular hypertrophy, whilst resumption of training increases the speed of ventricular relaxation in the presence of further hypertrophy of the left ventricle.
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Introduction
Vigorous exercise training induces hypertrophy of the left ventricle, an adaptation commonly referred to as ‘athlete's heart’ (Maron, 1986). In patients with cardiovascular disease, left ventricular (LV) hypertrophy is associated with diastolic dysfunction, characterized by impaired ventricular relaxation and filling which manifest on echocardiographic assessment as Doppler velocity abnormalities (Ommen & Nishimura, 2003). However, exercise training is cardioprotective, being associated with decreased cardiovascular mortality and morbidity in both primary (Paffenbarger et al. 1993; Blair et al. 1995) and secondary prevention settings (Joliffe et al. 2003) and, in contrast with the situation in patients with cardiovascular disease, LV hypertrophy associated with athletic training is likely to be a benign or beneficial adaptation which does not impact on ventricular relaxation in the same manner as ‘pathological’ hypertrophy. Previous studies indicate that, despite significant ventricular hypertrophy, athletes possess normal (MacFarlane et al. 1991; Yeater et al. 1996) or enhanced diastolic function (Douglas et al. 1986; George et al. 1999; Caso et al. 2000), compared to matched controls. However, these studies relied exclusively upon cross-sectional comparisons and, to our knowledge, no studies have investigated changes in LV diastolic function in athletes studied longitudinally in response to exercise training. The purpose of the current study was therefore to assess cardiac structural and functional adaptations to exercise training in elite level athletes across a typical training cycle, which is at the end of the ‘off-season’ and following 3 and 6 months of intensive training.
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Methods
Subject characteristics
Twenty-two elite rowers (17 male, 5 female) from the West Australian Institute of Sport were recruited into the ‘athlete’ group. The characteristics of these subjects were as follows (mean ± S.E.M.): age 20.4 ± 0.7 years, height 186.2 ± 1.0 cm, weight 81.5 ± 1.8 kg, body surface area (BSA) 2.06 ± 0.03 m2, mean resting heart rate (HR) 56 ± 2 b.p.m., resting systolic (SBP) 122 ± 2 mmHg, and resting diastolic blood pressure (DBP) 78 ± 2 mmHg.
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Twelve healthy controls matched for sex (8 male, 4 female), age 21.8 ± 1.1 years, height 183.9 ± 1.9 cm, weight 76.2 ± 3.1 kg, BSA 1.97 ± 0.04, resting HR 59 ± 2 b.p.m., SBP 123 ± 2 mmHg, and DBP 74 ± 3 mmHg, were recruited from the University of Western Australia for comparison.
Inclusion criteria for the athlete group were previous competition at national or international level, and inclusion in the Western Australian Institute of Sport elite rowing squad. Healthy controls were defined as individuals undertaking less than 3 h of regular exercise per week. All participants were screened for cardiac abnormalities and cardiovascular disease prior to entering the study. Subjects who smoked, were hypertensive, had a family history of hypertrophic occlusive cardiomyopathy or were on medications of any type were excluded, as were athletes on performance enhancing drugs.
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The study procedures were approved by the Ethics Committee of Royal Perth Hospital and all subjects gave written consent. The study conformed to the Declaration of Helsinki.
Experimental design
Athletes entered the study (baseline measures) at the beginning of their training cycle, that is, following the end of a 6 week ‘off season’ during which all formal training was suspended. Interviews were conducted to confirm that the athletes had not been training or exercising regularly during this ‘off-season’ phase; none of the subjects continued on-water training, 13 reported undertaking no exercise whatsoever, whilst the remaining nine performed relatively low intensity activity, none for more than 4 h per week; four reported undertaking intermittent jogging and five undertook school-based sport. To assess the effect of resumption of training, all measures were repeated following 3 and 6 months of training. Training in the athletes consisted of two sessions of exercise per day, 6–7 days per week. Morning sessions were ‘on water’ and consisted of 2.5 h training at, or near, competition pace, i.e. approx. 80–90% maximum heart rate (HRmax). Afternoon sessions were 2 h in duration and consisted of general aerobic conditioning (e.g. 12 km timed runs) or resistance training (80–90% 1RM (repetition maximum), 6–8 repetitions).
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The controls were recreationally active and healthy but did not undertake formal training for any sport, and their activity levels remained constant throughout the duration of the study. Data for the control group were collected at baseline, 3 months and 6 months to coincide with data collection in the athlete group.
Experimental measures
Two-dimensional ultrasound imaging, M-mode imaging and pulsed wave Doppler and flow propagation velocity (VP) measurements were used to assess resting cardiac structure and function in each subject. All measurements were performed following a 4-h fast, abstinence from caffeine and/or alcohol for 12 h and at least 18 h after physical activity. Echocardiographic assessments were collected and analysed by a trained sonographer (L.H.N.), who was not blinded. To check for systematic bias, a random sample of 30 of these scans were also assessed by a specialist echocardiologist (J.A.D.) who was uninformed as to subject group and session and had no direct contact with the subjects.
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Measures of cardiac structure. Left ventricular dimensions were measured using two-dimensional guided M-mode measurements on an ultrasound machine (Aspen, Acuson, Mountain View, CA, USA) equipped with a 2.5 MHz multiarray transducer. The mean value of at least five measurements of each dimension of the left ventricle was determined: interventricular septal thickness (IVS), left ventricular diastolic dimension (LVIDd), posterior wall thickness (PWT) and left ventricular systolic dimension (LVIDs). Left ventricular mass was calculated according to the recommendations of the American Society of Echocardiography (ASE):
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LV mass was indexed to BSA to calculate LV mass index (LVMi). Relative wall thickness (RWT), an indicator of LV geometry, often used to discriminate between different forms of LV hypertrophy (Roman et al. 1992), was calculated as 2 x (PWT/LVIDd).
Measures of cardiac systolic function. Stroke volume (SV), ejection fraction (EF) and fractional shortening (FS) were calculated using M-mode imaging to assess global function of the LV. Fractional shortening was estimated as the difference between systolic and diastolic ventricular dimensions (normalized to diastolic LVIDd). Stroke volume and EF were calculated from estimated LV volumes, with:
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Measures of cardiac diastolic function. The primary measure for diastolic function was colour M-mode Doppler flow propagation velocity (VP). VP measurements were obtained from apical four-chamber views, with the M-mode cursor as parallel as possible to flow obtained by colour Doppler, and the Doppler colour scale adjusted for aliasing. VP was recorded at a sweep speed of 100 mm s–1 and measured as the slope of first aliasing velocity in centimetres per second, with normal VP ranging between 68 and 105 cm s–1 (Anderson, 2000).
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Transmitral flow measurements were also made according to the ASE guidelines (Quinones et al. 2002; Gottdiener et al. 2004) and used as a secondary measure of diastolic function. Transmitral peak early filling velocity (Peak E), the deceleration time of early flow (DT) and peak velocity of atrial filling (Peak A) were measured, and the E/A ratio calculated.
Peak systolic (Peak S) and diastolic (Peak D), and atrial reversal (AR) velocities were also measured and the S/D ratio calculated from pulsed Doppler measures in the right upper pulmonary vein.
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Statistical analysis
Student's unpaired t test was used to assess significance between the controls and rowers at baseline. Two-way ANOVA was used to assess significance of difference (P < 0.05) between the athletes and controls across the three time points. One-way ANOVA was used within groups to determine whether variables changed with training, or across the non-training period in the case of controls. Where ANOVA revealed significant differences, post hoc t tests were used to compare individual time points. All data are reported as means ± S.E.M. and statistical significance was assumed at P < 0.05. All statistical analysis was performed using SPSS, version 11.0 (SPSS Inc., Chicago, IL, USA). Sub-group analysis on the male athletes revealed similar data to the group as a whole, so all data were pooled.
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The coefficient of variation (CV) for our primary outcome variable, VP, was 9.9%. This was calculated via assessment of the standard deviation of the differences between paired measurements at baseline and 3 months in the control subjects, division of this value by the square root of 2, and expression as a percentage of the mean value.
Results
Baseline cardiac structure
Compared to controls, athletes possessed structural adaptations consistent with ‘athlete's heart’; that is, increased LV mass (P < 0.01; Table 1, Fig. 1), with underlying increases in cavity dimension (LVIDd P < 0.01) and wall thicknesses (IVS and PWT, P < 0.01), but no significant differences in RWT between the groups (Table 1).
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Values are means ± S.E.M. The athletes possessed significantly increased LV mass (all P < 0.001) compared to the controls at all three time points. Compared to baseline measures, LV mass increased following 3 and 6 months training in the athlete group (P < 0.01, P < 0.05, respectively), but no changes occurred in LV mass in controls with time. *P < 0.001; P < 0.01; P < 0.05.
Baseline cardiac function
Stroke volume (SV) was the only measure of cardiac systolic function which significantly differed between athletes and controls at baseline (95.05 ± 2.78 ml versus 81.88 ± 2.53 ml; P < 0.05). Other indices of global LV systolic function were within normal ranges for both groups, with EF of 70 ± 1% and 72 ± 2% (athletes versus controls, not significant (NS)) and FS 39 ± 1% versus 42 ± 1% (NS).
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In terms of diastolic function, our primary measure (colour M-mode flow propagation velocity, VP) showed the largest differences between the groups at baseline (P < 0.001, Table 2), suggesting reduced diastolic filling parameters in the athletes. This was supported by increased deceleration times (DT; P < 0.01) with 10 athletes having DT measures greater than that defined as ‘normal’ (258 ms) (Munagala et al. 2003), whereas this was the case in only one control subject. The atrial reversal (AR) measured at the pulmonary veins also supported reduced diastolic parameters (P < 0.01). However, the E/A ratio, a preload dependent index (Ommen & Nishimura, 2003), which we measured purely to provide comparisons with previously published data, did not show any differences between groups (Table 2). Furthermore, the E/A ratio has been shown only to be accurate in predicting LV diastolic function in patients with systolic dysfunction, is non-specific and is influenced by many other factors, particularly in patients with preserved systolic function (such as this group of athletes) (Nishimura et al. 1996; Yamamoto et al. 1997).
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Effects of exercise training on cardiac structure
The athletes were highly motivated and compliance to the training program was excellent (98% across the period of the study, with no individual missing more than 20 out of 288 sessions). increased from 5.51 ± 0.20 at baseline to 5.64 ± 0.22 at 3 months and 5.68 ± 0.20 l min–1 at 6 months (both 3 and 6 months versus baseline P < 0.01).
Two-way ANOVA between athletes and controls at baseline and 3 months revealed significant differences in all indices of cardiac ‘structure’ (Table 1). This was indicated by increased measures in the athletes of LV mass, LVMi, IVS, PWT, and LVIDs following 3 months of training (Table 1). These findings were also evident following 6 months; LV mass, IVS, LVIDs and RWT remained significantly elevated relative to baseline measures (all P < 0.05). There were no significant differences in any measures of cardiac structure between the three time points in the control subjects.
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Effects of exercise training on cardiac function
Systolic function was not significantly altered by training in the athletes or across time in the control subjects (SV, SV index, EF and FS, all NS). However, indices of diastolic function were significantly augmented with the resumption of training, at 3 months VP, the S/D ratio and AR all differed compared to baseline measures (P < 0.05; Table 2, Fig. 2). Similar findings were evident for VP and AR following 6 months (P < 0.01; Table 2).
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Values are means ± S.E.M. The athletes possessed impaired VP compared to the controls at baseline (P < 0.001). VP improved with 3 months of training (P < 0.05 compared to controls), and normalized (NS, compared to controls) following 6 months of training. There were significant improvements in VP in the athlete group from baseline to 3 months (P < 0.001) and 6 months (P < 0.001), and from 3 to 6 months (P < 0.001). *P < 0.001; P < 0.01; P < 0.05.
At 3 months the athletes had significantly different VP, DT and S/D ratio measurements compared to the controls (all P < 0.05; Table 2). Following 6 months of training, there were no differences in any measures of diastolic function between the athletes and controls. There were no significant changes in any of the measures of diastolic function in controls between baseline, 3 or 6 months.
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Two-way ANOVA performed across the three study time-points between athletes and controls revealed a significant interaction term for VP (P < 0.001) and significant time (P < 0.05) and group (P < 0.0001) differences for LV mass.
Discussion
Our results indicate that athletes who are not currently active possess evidence of delayed early diastolic ventricular relaxation in concert with increased cardiac dimensions compared to matched controls. Following resumption of training for 3 months, we observed further increase in cardiac structure in the athletes, associated with augmented indices of diastolic relaxation. These changes persisted following 6 months of training, with measures of early diastolic filling reaching levels no longer statistically different from controls.
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Several previous studies have reporting increased cardiac dimensions (MacFarlane et al. 1991; Spirito et al. 1994; George et al. 1999; Pelliccia et al. 1999) in athletes. However, these studies used cross-sectional comparisons and the effects of training on cardiac structure and diastolic function in individual athletes remain unknown. We observed significantly increased LV dimensions and mass in athletes, which was further augmented following resumption of training. Our results also indicate increased SV in the presence of normal EF, reflecting the enlarged LV dimensions in athletes. These wall thickening and cavity enlargement results in rowers concur with previous cross-sectional comparisons in the literature (Finkelhor et al. 1986; Urhausen et al. 1996; Pelliccia & Maron, 1997; Pelliccia et al. 1999; Pelliccia et al. 2002), including a study which suggested that LV hypertrophy persists after long-term detraining in elite athletes (Pelliccia et al. 2002). It is interesting to note in the present study that, despite marked physiological hypertrophy relative to matched controls at the end of the ‘off-season’ in athletes, resumption of training induced further, significant increases in LV mass. This finding is consistent with a recent study which assessed serial left ventricular structural adaptations in cyclists (Abergel et al. 2004), indicating that individuals with existing evidence of ‘athlete's heart’ can undergo further cardiac enlargement as a result of the further exercise training.
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We describe, for the first time, reduced flow propagation velocity in athletes following their ‘off-season’. Although all measures of diastolic function are preload dependent, VP is relatively insensitive to changes in preload (Brun et al. 1992; Garcia et al. 1999) compared to the E/A ratio (Gottdiener et al. 2004) and tissue Doppler echocardiographic (TDI) indices (Firstenberg et al. 2001) and correlates closely with (Garcia et al. 2000), the time constant for isovolumetric ventricular relaxation. This reduction in VP relative to controls, supported by transmitral DT and pulmonary venous AR measures, indicates that the enlarged LV dimensions evident in athletes are associated with delayed diastolic filling when athletes are not currently engaged in training. Furthermore, our findings indicate that resumption of physical activity results in improvement in diastolic filling in athletes, in the presence of further cardiac enlargement and wall thickening. Previous reports, which have predominantly undertaken cross-sectional comparisons between athletes and controls using the E/A ratio, have interpreted their data as indicating either normal or enhanced diastolic function in athletes (Douglas et al. 1986; MacFarlane et al. 1991; George et al. 1999). Our data are not entirely inconsistent with these studies, as exercise training significantly improved VP in the athletes and the athletes possessed similar diastolic function to controls when they were training. Nonetheless, our finding of delayed early diastolic filling in athletes at entry, when they were relatively inactive, differs from previous studies which have reported enhanced diastolic function. Several possible explanations exist for the disparity. Firstly, all previous studies have utilized cross-sectional designs and have not specifically reported at what stage of the training cycle athletes were studied. This is relevant given our VP data strongly indicate that early diastolic filling was initially reduced when the athletes were not active, whereas progressive normalization occurred with training. A second possible explanation may relate to the indices of diastolic function used. Previous studies have typically relied upon the E/A ratio, which has several important limitations including preload dependence (Ommen & Nishimura, 2003), which may be of particular relevance in athletes in whom plasma volume and preload may be enhanced by training.
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Whilst the Doppler measures we report in this paper are typically those assessed in the clinical setting (Gottdiener et al. 2004), we think it unlikely that the impaired VP, DT and AR data we observed in the inactive athletes are indicative of diastolic dysfunction in these subjects, who are young, healthy and capable of performing at extremely high levels. We do not have evidence that the heart fills inadequately, or at higher pressures than normal or that it cannot sustain higher levels of venous return during exercise and it would therefore be inappropriate to infer diastolic ‘dysfunction’ from the clinical setting. Furthermore, previous studies indicate that exercise training improves ventricular compliance (Levine et al. 1991) and, although chronic inactivity associated with bed rest and space flight are associated with impaired compliance (Perhonen et al. 2001a; Perhonen et al. 2001b), this degree of activity restriction is not relevant to our study. Ultimately though, our data do indicate that propagation velocity is slowed following a period of detraining and raise interesting questions regarding mechanisms. Propagation velocity is dependent upon atrioventricular pressure gradients, the relationship between end-systolic volume and equilibrium volume and the rate of relaxation in early diastole. It is possible that any or all of these determinants were altered in the present study; for example, decreased plasma volume as a consequence of detraining, in the presence of sustained ventricular enlargement, may have decreased equilibrium volume to the point where early diastolic suction and flow propagation were decreased. This explanation is speculative and others may exist; future studies incorporating new and evolving technologies, such as myocardial tissue Doppler imaging and cardiac MRI will provide further valuable information regarding the effects of exercise on LV structure and diastolic filling. Functional assessment of ventricular compliance and construction of Starling curves (Levine et al. 1991) during different phases of athletic training cycles would be particularly revealing, although ethical concerns in elite athletes may limit such invasive investigations.
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There are several limitations of the present study. It is well established that Doppler measures of diastolic function are HR dependent and training-induced changes or differences between controls and athletes may be partly dependent upon differences in HR. However, the athletes and controls were well matched for resting HR and no significant changes in HR were observed across the training programme in the athletes. Furthermore, the slight decrease in resting HR with training in the athletes would not be expected to increase VP, as observed at 3 and 6 months. A second possible limitation relates to the measures of diastolic function we reported. As mentioned above, we have attempted to present those measures which we believe are the most valid, given the limitations of Doppler approaches. VP is the Doppler approach recommended to assess diastolic function by the American Society of Echocardiography as it is less subject to ‘pseudonormalization’ and correlates better with than other measures (Garcia et al. 2000; Gottdiener et al. 2004). Furthermore, VP appears less preload dependent than tissue Doppler measures (Garcia et al. 2000; Firstenberg et al. 2001). Finally, several echocardiographic approaches exist to assess LV mass. We adopted the algorithm recommended for use in conjunction with linear measures of ventricular wall thickness and cavity dimensions (Gottdiener et al. 2004). Such measures are subject to limitations associated with oblique parasternal imaging, but in subjects with normal geometry the approach we adopted is preferred to the use of Simpson's rule due to difficulty identifying boundaries of the LV free wall from base to apex in apical windows (Gottdiener et al. 2004). Reproducibility of the approach we used is acceptable given careful attention to image quality and assessment of primary dimensions (Gottdiener et al. 2004) and we think it unlikely that the relatively small training-induced change in LV mass we observed in athletes is the result of a type 2 error as both the 3 and 6 month data increased consistently and no change was observed in the parallel control group over time. Furthermore, the magnitude of increase in LV mass we report is similar to, or greater than, that previously reported as significant as a result of other interventions (Poppas et al. 1997; Mesa et al. 1999; Modena et al. 1999; Mayet et al. 2000).
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In summary, data from the present study imply that following a period of relative inactivity, the rate of ventricular relaxation during early diastole may be slowed in athletes who exhibit ventricular hypertrophy, whilst resumption of training increases the speed of ventricular relaxation in the presence of further hypertrophy of the LV.
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